Inhibiting protein may provide balance in lupus treatment

Treating autoimmune diseases is tricky, said OMRF scientist Darise Farris, Ph.D. Because symptoms of the disease vary so widely among patients, and even in individuals, doctors often find these conditions challenging to manage.

“The therapy for many patients with lupus or Sjögren’s syndrome is to suppress the immune system,” she said. “If you suppress too much, the patients are open to infections. But if you don’t do enough, they can be harmed by the resulting inflammation.”

A new paper from Farris and OMRF scientist Chris Horton, Ph.D., explains how controlling a protein called Interleukin 6, or IL-6, might help find that balance.

It is estimated that autoimmune diseases, including lupus, Sjögren’s, type 1 diabetes and rheumatoid arthritis, affect as many as 22 million Americans. In these conditions the immune system becomes unbalanced and proteins or cells that would normally protect from harmful invaders begin attacking the body’s own tissues.

Using a mouse model that mimics lupus and Sjögren’s, Farris and Horton knocked out the IL-6 protein and found the mice had no signs of autoimmune disease. Without the protein, the mice didn’t create auto-antibodies—immune cell products that turn against the host—and kept immune cells from penetrating salivary gland tissue and the kidneys.

“That doesn’t mean we should get rid of IL-6 altogether,” Horton said. “It’s a protein that is important in the development of the immune system, including helper T cells, which fight infections. But when there’s too much of it, it causes problems for patients.”

Farris said the research comes at a great time, as pharmaceutical companies are currently testing a drug that inhibits IL-6.

“Finding a method to keep the protein at a normal level might be one way to balance the immune system in autoimmune disease patients,” Farris said.

Their work was published in the journal Arthritis & Rheumatology.

OMRF researcher Mark Coggeshall, Ph.D., and University of Texas at El Paso scientist Jacen Moore, Ph.D., contributed to the research.

Funding was provided by grants No. R01 AI048097 from the National Institute of Allergy and Infectious Diseases, P50 AR060804 and T32 AI007633 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, part of the National Institutes of Health.